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SRPS Volume 10, Number 7, Part 1<br />

cell to radiation damage is directly proportional to<br />

its mitotic rate. The most sensitive cells are those<br />

which divide rapidly, such as cells of the skin, bone<br />

marrow, and gastrointestinal tract. In addition to<br />

sensitivity of the exposed cell, morbidity from<br />

radiation depends on the dose received, time over<br />

which the dose is received, volume of tissue irradiated,<br />

and type of radiation. 399 Cellular changes<br />

resulting from low-dose radiation are probably due<br />

to an apoptotic mechanism, whereas changes<br />

related to high-dose radiation are probably due to<br />

direct cellular necrosis.<br />

The direct effects of radiation can be immediate,<br />

acute (days to weeks), or delayed (months to<br />

years). Acute effects result from necrosis of the rapidly<br />

proliferating cell lines. A transient, faint erythema<br />

may appear during the first week of treatment due<br />

to dilation of capillaries and may be associated with<br />

an increase in vascular permeability. Radiation<br />

inhibits mitotic activity in the germinal cells of the<br />

epidermis, hair follicles, and sebaceous glands. Epilation<br />

and dryness of the skin occur. By the third or<br />

fourth week of radiation, typical erythema is localized<br />

to the radiation field and the skin is noticeably<br />

red, edematous, warm, and tender. Larger vessels<br />

may be obstructed by fibrin thrombi, edema is<br />

prominent, and there may be small foci of hemorrhage.<br />

400 Cellular exudate is rare. If the total radiation<br />

dose to the skin does not exceed 30Gy, the<br />

erythema phase is followed during the fourth or<br />

fifth week by a dry desquamation phase characterized<br />

by pruritus, scaling, and an increase in melanin<br />

pigmentation in the basal layer. Within 2 months<br />

the inflammatory exudate and edema have subsided,<br />

leaving an area of brown pigmentation.<br />

If the total radiation dose to the skin is >40Gy,<br />

the erythema phase is followed by a moist desquamation<br />

phase. This stage usually begins in the fourth<br />

week and is often accompanied by considerable<br />

discomfort. Bullous formation occurs above the basal<br />

layer and sometimes just below the epidermis. Eventually<br />

the roofs of the bullae are shed and the entire<br />

epidermis may be lost in portions of the irradiated<br />

area. Edema and fibrinous exudate persist. In the<br />

absence of infection, reepithelization of the<br />

denuded skin usually begins within 10 days. Ulcers<br />

may appear 2 weeks or more after radiation exposure.<br />

These ulcers are a result of direct necrosis of<br />

the epidermis; they usually heal but tend to<br />

recur. 399,401<br />

Approximately 1 year after radiation treatment<br />

the epidermis is thin, dry, and semitranslucent, with<br />

vessels easily seen. Hair follicles and sebaceous<br />

glands are usually absent. Some sweat glands may<br />

also have been destroyed. In time, increasing fibrosis<br />

of the skin is present. Much of the collagen and<br />

subcutaneous adipose tissue are replaced by atypical<br />

fibroblasts and dense fibrous tissue that may<br />

cause induration of the skin and may limit movement.<br />

In radiation injury of soft tissue, fibrinous<br />

exudate accumulates under the epidermis. Characteristic<br />

features of delayed radiation lesions are<br />

eccentric myointimal proliferation of the small<br />

arteries and arterioles as well as telangiectasia. These<br />

changes may progress to thrombosis or complete<br />

obstruction. Delayed ulcers are more common than<br />

acute ulcers and result from ischemic changes in<br />

small arteries and arterioles; they heal slowly and<br />

may persist for several years. Irradiated skin in the<br />

chronic stage is thin, hypovascularized, extremely<br />

painful, and easily injured by any slight trauma or<br />

infection. 399,401<br />

Skin reactions to radiation should be treated early<br />

to prevent complications later. Keeping the skin<br />

moist and pliable to prevent fissures and cracks and<br />

free of infection is extremely important. Mendelsohn<br />

et al 402 has compiled a list of products to treat<br />

radiation-induced skin changes (Table 10). If an<br />

ulcer develops, the normal <strong>wound</strong> care protocols<br />

should be initiated. In severe cases, wide<br />

debridement and a skin graft or flap coverage may<br />

be necessary.<br />

Treatment with hyperbaric oxygen accelerates<br />

<strong>healing</strong> in some patients, 403,404 but its effectiveness<br />

in soft-tissue necrosis from radiation injury is<br />

unproven. Experimental therapies include topical<br />

TGF-β1, 405 granulocyte-macrophage colonystimulating<br />

factor (GM-CSF), 406 orgotein (a Cu/Zn<br />

chelate with superoxide dismutase), 407 topical vitamin<br />

C, 408,409 topical corticosteroids, 410 glucorticoids,<br />

411 NSAIDs, 412 aloe vera gel, 413,414 heliumneon<br />

laser treatments, 415 and oral pentoxifylline<br />

treatment. 416<br />

HIGH-PRESSURE INJECTION INJURIES<br />

High-pressure injection devices such as are used<br />

for painting, cleaning, degreasing, etc. can produce<br />

pressures of 600–12,000psi. 417,418 The substance<br />

enters the skin through a seemingly insignificant<br />

35

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